Osteoarthritis (OA) is a disease of synovial joints (Fig. 7.1) and is the most common form of arthritis.
The prevalence of OA increases with age, and most people over 60 years will have some radiological evidence of it although only a proportion of these have symptoms. OA occurs world-wide, it is more common in women and there is a familial tendency to develop nodal and generalized OA. Other risk factors are obesity, a fracture through a joint, congenital joint dysplasias, pre-existing joint damage of any cause, occupation (e.g. OA of the hip in farmers and labourers) and repetitive use and injury associated with some sports.
Pathology and pathogenesis
OA is the result of active, sometimes inflammatory but potentially reparative processes, rather than the inevitable result of trauma and ageing. It charac-terized by progressive destruction and loss of articular cartilage with an accompanying periarticular bone response. The exposed subchondral bone becomes sclerotic, with increased vascularity and cyst formation. Attempts at repair produce cartilaginous growths at the margins of the joint which later become calcified (osteophytes).
Several mechanisms have been suggested for the pathogenesis:
■ Metalloproteinases, e.g. stromelysin and collagenase, secreted by chondrocytes degrade collagen and proteoglycans.
■ Interleukin (IL)-1 and tumour necrosis factor (TNF)-a stimulate metallo-proteinase production and inhibit collagen production.
■ Deficiency of growth factors such as insulin-like growth factor and trans-forming growth factor impairs matrix repair.
■ Genetic susceptibility (35-65% influence) from multiple genes rather than a single gene defect. Mutations in the gene for type II collagen have been associated with early polyarticular OA.
Most OA is primary with no obvious predisposing factor. Secondary OA occurs in joints that have been damaged in some way or are congenitally abnormal.
Joint pain is the main symptom, made worse by movement and relieved by rest. Stiffness occurs after rest (‘gelling') and in contrast to inflammatory arthritis there is only transient (<30 minutes) morning stiffness. The joints most commonly involved are the distal interphalangeal joints (DIPJs) and first carpometacarpal joint of the hands, first metatarsophalangeal joint of the foot and the weight-bearing joints - vertebrae, hips and knees. Elbows, wrists and ankles are rarely affected. On examination there is deformity and bony enlargement of the joints, limited joint movement and muscle wasting of surrounding muscle groups. Crepitus (grating) is a common finding and is probably due to the disruption of the normally smooth articulating surfaces of the joints. There may be a joint effusion. Heberden's nodes are bony swellings at the DIPJs. Bouchard's nodes are similar but occur at the proximal IPJs (Fig. 7.2).
OA is differentiated from RA by the pattern of joint involvement and the absence of the systemic features and marked early morning stiffness that occur in RA. A chronic arthropathy (pseudo-OA) occurs, predominantly in
Fig. 7.2 Severe nodal osteoarthritis (OA). The distal interphalangeal (DIP) joints demonstrate Heberden’s nodes (arrows). The middle finger DIP joint is deformed and unstable. The thumb is adducted and the bony swelling of the first carpometacarpal joint is clearly shown - ‘the squared hand of nodal OA’.
elderly women with severe chondrocalcinosis (p. 296) but the wrists and shoulder are usually involved and the hands rarely involved. Chronic tophaceous gout (p. 293) and psoriatic arthritis affecting the DIPJs (p. 292) may mimic OA.
■ Full blood count and ESR are normal. Rheumatoid factor is negative, but positive low-titre tests may occur incidentally in elderly people.
■ X-rays are only abnormal in advanced disease and show narrowing of the joint space (resulting from loss of cartilage), osteophytes, subchondral sclerosis and cyst formation.
■ MRI demonstrates early cartilage changes. It is not necessary for most patients with suggestive symptoms and typical plain X-ray features.
Treatment should focus on the symptoms and disability, not the radiological appearances. Patient education about the disease, non-pharmacological measures, drugs and surgery all have a role. Obese patients should be encouraged to lose weight, particularly if weight-bearing joints are affected.
■ Physical measures are the keystone of OA treatment. Local strengthening and aerobic exercises improve local muscle strength, improve the mobil-ity of weight-bearing joints and improve general aerobic fitness. Local heat or ice packs applied to an affected joint may also help. Bracing devices, joint supports, insoles for joint instability and footwear with shock-absorbing properties for lower limb OA are also used. A walking stick held on the contralateral side to the affected lower limb joint is useful. Acupuncture helps knee OA.
■ Medication. Paracetamol (p. 317) is the initial drug of choice for pain relief, with the addition of a weak opioid, e.g. dihydrocodeine (p. 317), if neces-sary. NSAIDs (p. 317), e.g. ibuprofen or coxibs are used in patients who do not respond to simple analgesia and should be used in short courses rather than a continuous basis. NSAIDs can also be given topically. Intra-articular corticosteroid injections produce short-term improvement when there is a painful joint effusion; systemic corticosteroids are not used.
■ Surgery. Total hip and knee replacement has transformed the manage-ment of severe symptomatic OA. There is reduced pain and stiffness and an associated increase in function and mobility. Complication rates are low with loosening and late bone infection being the most serious.
1. Ethics and communication
2. Infectious diseases
3. Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER DISEASE IN PREGNANCY
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS
5. Haematological disease
Assessment and treatment of suspected neutropenic sepsis
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
6. Malignant disease
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
8. Water, electrolytes and acid–base balance
WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
9. Renal disease
INVESTIGATION OF RENAL DISEASE
URINARY TRACT INFECTION
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
10. Cardiovascular disease
COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
ISCHAEMIC HEART DISEASE
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
ARTERIAL AND VENOUS DISEASE
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS
11. Respiratory disease
12. Intensive care medicine
13. Drug therapy, poisoning, and alcohol misuse
14. Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
15. Diabetes mellitus and other disorders of metabolism
16. The special senses
COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES